A mutation in the APC (adenomatous polyposis coli) antioncogene, which has been identified as a genetic cause of familial adenomatous polyposis, is a mutation which takes place early in the oncogenic pathways of not only familial adenomatous polyposis but also of sporadic colon cancer, and it is a very common genetic mutation seen in more than 80% of cases.
It is known that a mutation of this APC antioncogene leads to the intracellular accumulation of β-catenin. This β-catenin combines with a transcription factor of the TCF/LEF family, and leads to transcriptional activity. In many cases of colon cancer, in the TCF/LEF family, cell biology changes arise in the intestinal epithelium due to the transcriptional activation of T-cell factor-4 (TCF4) which affects the control of differentiation of the intestinal epithelium. It is thought that, subsequently, this forms an early colon adenoma and results in oncogenic transformation through a secondary multi-stage genetic mutation.
Since a mutation of the β-catenin gene is seen in about half of the cases wherein there is no genetic mutation of APC, compounds which inhibit the function of the transcription complex of β-catenin and TCF4 (β-catenin/TCF4 transcription complex) are viewed as a promising a new molecular therapeutic drug for colon cancer.
In this context, therapeutic drugs that, by binding with β-catenin, have an inhibitory action on transcriptional activation when β-catenin combines with TCF/LEF family proteins to form complexes, have been proposed (Patent document 1).    Patent document 1: International publication 00/No. 64933
However, a satisfactory effective compound had not yet been developed, and it was therefore desired to develop an effective molecular therapy for colon cancer.